formed but only when other tests are inconclusive since it is more invasive.
The patient is required to fast overnight, then drink a solution containing 50 g
lactose. Several blood samples are taken over a 2-h period and their glucose
concentrations determined. The amount of blood glucose indicates how well
the patient is able to digest lactose. The test must be controlled by repeating
the procedure using 25 g each of glucose and galactose, the constituent mono-
saccharides of lactose.
The medical history, age, degree of intolerance and overall health of the
patient determine treatment for lactose intolerance. In general, it can be
controlled with an appropriate diet. Adding proprietary products containing
lactase (Figure 11.32) isolated from microorganisms to dairy products prior to
ingestion can also help overcome the problem.
Celiac disease is a genetically determined chronic inflammatory condition
affecting the small intestine and is induced by the ingestion of wheat pro-
tein, specifically gluten, and its products. A portion of the gluten molecule
forms an autoimmune complex in the GIT mucosa which stimulates T cells
to aggregate and release toxins that promote lysis of enterocytes (Chapters
4 and 5 ). This leads to a progressive atrophy and characteristic flattening of
the mucosal villi and microvilli in the upper part of the small intestine (Figure
11.33(A) and (B)). Celiac disease is a relatively common disorder with a
worldwide prevalence of 1 in 200–300. The mucosa improves morphologically
when the patient is placed on a gluten-free diet but relapses occur if gluten
is reintroduced in the diet. Celiac disease is accompanied by malabsorption
of nutrients due to a decreased surface area over which absorption can take
place. The signs and symptoms of celiac disease are surprisingly diverse and
include abdominal pain, chronic diarrhea, weight loss, bone pain, fatigue and
anemia. Celiac disease is diagnosed by demonstrating villous atrophy in a
small intestine biopsy (Figure 11.34 (A) and (B)) and by improvements in clini-
cal symptoms or histological tests following restriction to a gluten-free diet.
Gluten-free foods are now readily available in supermarkets and health food
stores. The management of celiac disease involves adherence to a gluten-free
diet, which in most cases helps relieve the symptoms and allows the existing
mucosal damage to heal as well as preventing further damage.
Malabsorption is a reduction in the absorption of one or more nutrients by the
small intestine. It occurs as a result of a wide range of disorders that affect the
GIT, pancreas, liver and gall bladder. Its causes include enzyme deficiencies,
such as in lactose intolerance, chronic pancreatitis, bile salt deficiency, as in
biliary obstruction or hepatitis, and intestinal diseases such as celiac disease
and Crohn’s disease (see below). The clinical features of malabsorption (Figure
11.35) arise because of deficiency of one or more nutrients and include anemia
due to iron, folate and vitamin B 12 deficiencies, osteomalacia due to vitamin D
deficiency, edema due to hypoalbuminemia, the tendency to bleeding when
vitamin K is suboptimal and generalized weight loss. Malabsorption results in
retention of nutrients in the GIT lumen causing diarrhea and abdominal dis-
comfort due to the action of GIT bacteria. Malabsorption of fats leads to their
losses in amounts greater than 5 g daily and causes steatorrhea. The feces are
greasy, with a pale color and have an offensive smell.
A diseased liver may be unable to synthesize bile which is required for diges-
tion of fats and if absent can lead to malabsorption. Liver function tests can
indicate the presence of liver disease and a number of blood tests are also use-
ful in assessing liver function. These include determining the concentration
of albumin in the plasma and hematological investigations such as full blood
count, iron, vitamin B 12 and folate and can indicate the type of malabsorption.
Investigations of malabsorption also include microbiological examination of
feces to identify any pathogens present. The pentose sugar xylose is absorbed
in the small intestine but is not metabolized and is excreted unchanged in
DISORDERS OF THE GIT AND ACCESSORY ORGANSCZhhVg6]bZY!BVjgZZc9Vlhdc!8]g^hHb^i]:YLddY (%,
Figure 11.32A proprietary product containing
lactase used for the digestion of lactose prior to
ingestion.Figure 11.33Photomicrographs of (A) healthy
villi (V) and associated crypts of Lieberkuhn (C)
and (B) the mucosal lining from a celiac patient.
Note the degeneration of the villi.